Raz Itamar, Eldor Roy, Naparstek Yaakov
Diabetes Research Center, Department of Medicine, Hadassah-Hebrew University Hospital, Jerusalem 91120, Israel.
Trends Biotechnol. 2005 Mar;23(3):128-34. doi: 10.1016/j.tibtech.2005.01.009.
Prevention of type 1 diabetes mellitus requires early intervention in the autoimmune process directed against beta cells of the pancreatic islets of Langerhans. This autoimmune inflammatory process is thought to be caused by the effect of Th1 cells and their secreted cytokines (e.g. interferon) and to be suppressed by Th2-secreted anti-inflammatory cytokines (e.g. IL-4, IL-10). Various methods aimed specifically at halting or modulating this response have been attempted. An alternative method is the re-induction of tolerance towards the putative self antigen that causes the disease. Proposed antigens such as insulin, glutamic acid decarboxilase (GAD) and the heat shock protein 60 (Hsp60)-derived peptide 277 have been used successfully in murine diabetes models and in initial clinical trials in early diabetes patients. Here, we review the results of these trials.
1型糖尿病的预防需要在针对朗格汉斯胰岛β细胞的自身免疫过程中进行早期干预。这种自身免疫性炎症过程被认为是由Th1细胞及其分泌的细胞因子(如干扰素)的作用引起的,并被Th2分泌的抗炎细胞因子(如IL-4、IL-10)所抑制。已经尝试了各种专门旨在阻止或调节这种反应的方法。另一种方法是重新诱导对引发该疾病的假定自身抗原的耐受性。诸如胰岛素、谷氨酸脱羧酶(GAD)和热休克蛋白60(Hsp60)衍生肽277等提出的抗原已在小鼠糖尿病模型和早期糖尿病患者的初步临床试验中成功使用。在此,我们综述这些试验的结果。